Evidence map›Paper›PMID 34663205›Full record

ArticleThe journal of physiological sciences : JPS2021

Shen Qi Li Xin formula improves chronic heart failure through balancing mitochondrial fission and fusion via upregulation of PGC-1α.

Yan-Bo Sui, Jian Xiu, Jin-Xuan Wei, Pei-Pei Pan, Bi-Hong Sun, Li Liu

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in The journal of physiological sciences : JPS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 21 citations in OpenAlex.

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  13. PGC-1Frontiers in cell and developmental biology · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Yan-Bo Sui *Department of Cardiology, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, No 26 Heping Road, Xiangfang District, Harbin, 150040, China.
Jian Xiu *Department of Cardiology, First People's Hospital of Zhaoqing, No 9 Donggangdong Road, Duanzhou District, Zhaoqing, China.
Jin-Xuan WeiDepartment of Cardiology, Heilongjiang University of Chinese Medicine, No 24 Heping Road, Xiangfang District, Harbin, 150040, China.
Pei-Pei PanDepartment of Cardiology, Heilongjiang University of Chinese Medicine, No 24 Heping Road, Xiangfang District, Harbin, 150040, China.
Bi-Hong SunDepartment of Cardiology, Heilongjiang University of Chinese Medicine, No 24 Heping Road, Xiangfang District, Harbin, 150040, China. sunbih0@outlook.com.
Li LiuDepartment of Cardiology, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, No 26 Heping Road, Xiangfang District, Harbin, 150040, China. liuli_hucm@126.com.
Heilongjiang University of Chinese Medicine · CNFirst Affiliated Hospital of Heilongjiang University of Chinese Medicine · CNThe First People's Hospital of Zhaoqing · CN

Funding

heilongjiang postdoctoral scientific research developmental fund LBH-Q18118national natural science foundation of china 81904107
6 · The paper itself

Abstract

backgroundOur previous study proved that Shen Qi Li Xin formula (SQLXF) improved the heart function of chronic heart failure (CHF) patients, while the action mechanism remains unclear.

methodsH&E staining and TUNEL staining were performed to measure myocardial damages. Western blot was used to examine the expression of proteins. Moreover, CCK-8 assay and flow cytometry were used to measure cell viability and cell apoptosis, respectively. Concentrations of ATP and ROS in cells, and mitochondrial membrane potential (MMP) were detected to estimate oxidative stress.

resultsIn vivo, we found that SQLXF improved cardiac hemodynamic parameters, reduced LDH, CK-MB and BNP production, and attenuated myocardial damages in CHF rats. Besides, SQLXF promoted mitochondrial fusion-related proteins expression and inhibited fission-related proteins expression in CHF rats and oxygen glucose deprivation/reoxygenation (OGD/R)-induced cardiac myocytes (CMs). In vitro, our data show that certain dose of SQLXF inhibited OGD/R-induced CMs apoptosis, cell viability decreasing and oxidative stress.

conclusionOverall, certain dose of SQLXF could effectively improve the cardiac function of CHF rats through inhibition of CMs apoptosis via balancing mitochondrial fission and fusion. Our data proved a novel action mechanism of SQLXF in CHF improvement, and provided a reference for clinical.

Indexed as

Heart FailureMitochondrial DynamicsAnimalsApoptosisHumansMembrane Potential, MitochondrialMyocytes, CardiacRatsUp-RegulationCardiac functionChronic heart failureMitochondrial fissionMitochondrial fusionShen Qi Li Xin formula

Identifiers

PMID34663205
PMCPMC10717454
OpenAlexW3206104620

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.